{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,7]],"date-time":"2026-05-07T14:15:58Z","timestamp":1778163358722,"version":"3.51.4"},"reference-count":47,"publisher":"Rockefeller University Press","issue":"2","content-domain":{"domain":["rupress.org"],"crossmark-restriction":true},"short-container-title":[],"published-print":{"date-parts":[[2006,2,20]]},"abstract":"<jats:p>The major histocompatibility complex (MHC) class Ib molecule H2-M3 primes the rapid expansion of CD8+ T cells by presenting N-formylated bacterial peptides. However, the significance of H2-M3\u2013restricted T cells in host defense against bacteria is unclear. We generated H2-M3\u2013deficient mice to investigate the role of H2-M3 in immunity against Listeria monocytogenes (LM), a model intracellular bacterial pathogen. H2-M3\u2013deficient mice are impaired in early bacterial clearance during primary infection, with diminished LM-specific CD8+ T cell responses and compromised innate immune functions. Although H2-M3\u2013restricted CD8+ T cells constitute a significant proportion of the anti-listerial CD8+ T cell repertoire, the kinetics and magnitude of MHC class Ia\u2013restricted T cell responses are not altered in H2-M3\u2013deficient mice. The fact that MHC class Ia\u2013restricted responses cannot compensate for the H2-M3\u2013mediated immunity suggests a nonredundant role of H2-M3 in the protective immunity against LM. Thus, the early H2-M3\u2013restricted response temporally bridges the gap between innate and adaptive immune responses, subsequently affecting the function of both branches of the immune system.<\/jats:p>","DOI":"10.1084\/jem.20051866","type":"journal-article","created":{"date-parts":[[2006,2,14]],"date-time":"2006-02-14T01:33:44Z","timestamp":1139880824000},"page":"449-459","update-policy":"https:\/\/doi.org\/10.1084\/jem.crossmarkpolicy","source":"Crossref","is-referenced-by-count":44,"title":["Impaired response to <i>Listeria<\/i> in H2-M3\u2013deficient mice reveals a nonredundant role of MHC class Ib\u2013specific T cells in host defense"],"prefix":"10.1084","volume":"203","author":[{"given":"Honglin","family":"Xu","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Chicago, Chicago, IL 60637"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Taehoon","family":"Chun","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Chicago, Chicago, IL 60637"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Hak-Jong","family":"Choi","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Chicago, Chicago, IL 60637"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Bin","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Chicago, Chicago, IL 60637"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Chyung-Ru","family":"Wang","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Chicago, Chicago, IL 60637"}],"role":[{"role":"author","vocabulary":"crossref"}]}],"member":"291","published-online":{"date-parts":[[2006,2,13]]},"reference":[{"key":"2023072513324733100_BIB1","doi-asserted-by":"crossref","first-page":"383","DOI":"10.1038\/306383a0","volume":"306","year":"1983","journal-title":"Nature."},{"key":"2023072513324733100_BIB2","doi-asserted-by":"crossref","first-page":"971","DOI":"10.1016\/0092-8674(90)90345-F","volume":"60","year":"1990","journal-title":"Cell."},{"key":"2023072513324733100_BIB3","doi-asserted-by":"crossref","first-page":"335","DOI":"10.1016\/0092-8674(91)90623-7","volume":"66","year":"1991","journal-title":"Cell."},{"key":"2023072513324733100_BIB4","doi-asserted-by":"crossref","first-page":"1917","DOI":"10.1093\/intimm\/6.12.1917","volume":"6","year":"1994","journal-title":"Int. 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